ArticleThe Journal of physiology1999
Activation of a Ca2+-permeable cation channel by two different inducers of apoptosis in a human prostatic cancer cell line.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 47 citations in OpenAlex.
- Regulation of ADAM10 activity through microdomain-dependent intracellular calcium changes.Cell communication and signaling : CCS · 2024Article
- Changes in Electrical Capacitance of Cell Membrane Reflect Drug Partitioning-Induced Alterations in Lipid Bilayer.Micromachines · 2023Article
- Article
- Intracellular calcium oscillations in strongly metastatic human breast and prostate cancer cells: control by voltage-gated sodium channel activity.European biophysics journal : EBJ · 2016Article
- ARP2, a novel pro-apoptotic protein expressed in epithelial prostate cancer LNCaP cells and epithelial ovary CHO transformed cells.PloS one · 2014Article
- Non-THC cannabinoids inhibit prostate carcinoma growth in vitro and in vivo: pro-apoptotic effects and underlying mechanisms.British journal of pharmacology · 2013Article
- Functional coupling between large-conductance potassium channels and Cav3.2 voltage-dependent calcium channels participates in prostate cancer cell growth.Biology open · 2013Article
- Transient receptor potential melastatin 4 and cell death.Pflugers Archiv : European journal of physiology · 2012Review
- Pharmacological and functional properties of TRPM8 channels in prostate tumor cells.Pflugers Archiv : European journal of physiology · 2011Article
- Proapoptotic role of novel gene-expression factors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2007Review
- Potential roles of electrogenic ion transport and plasma membrane depolarization in apoptosis.The Journal of membrane biology · 2006Review
- BKCa channels activating at resting potential without calcium in LNCaP prostate cancer cells.The Journal of membrane biology · 2005Article
- ARP2 a novel protein involved in apoptosis of LNCaP cells shares a high degree homology with splicing factor Prp8.Molecular and cellular biochemistry · 2005Article
- Voltage-gated Na+ channels confer invasive properties on human prostate cancer cells.Pflugers Archiv : European journal of physiology · 2004Article
- Expression of Drosophila Ca2+ permeable transient receptor potential-like channel protein in a prostate cancer cell line decreases cell survival.Cancer gene therapy · 2003Article
- SERCA pump optimizes Ca2+ release by a mechanism independent of store filling in smooth muscle cells.Biophysical journal · 2003Article
- Voltage-dependent ion channel currents in putative neuroendocrine cells dissociated from the ventral prostate of rat.Pflugers Archiv : European journal of physiology · 2003Article
- Mitochondrial stress-induced calcium signaling, phenotypic changes and invasive behavior in human lung carcinoma A549 cells.Oncogene · 2002Article
- Store depletion and store-operated Ca2+ current in human prostate cancer LNCaP cells: involvement in apoptosis.The Journal of physiology · 2000Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We have combined patch clamp recording with simultaneous [Ca2+]i measurements in single LNCaP cells (a human prostate cancer cell line), to study the activation of Ca2+-permeable channels by two different inducers of apoptosis, ionomycin and serum deprivation. 2. In perforated patch recording, LNCaP cells had a membrane potential of -40 mV and a resting [Ca2+]i of 90 nM. Application of ionomycin at levels that induced apoptosis in these cells (10 microM) produced a biphasic increase in [Ca2+]i. The first rise in [Ca2+]i was due to release of Ca2+ from internal stores and it was associated with a membrane hyperpolarization to -77 mV. The latter was probably due to the activation of high conductance, Ca2+- and voltage-dependent K+ channels (maxi-K). Conversely, the second rise in [Ca2+]i was always preceded by and strictly associated with membrane depolarization and required external Ca2+. Serum deprivation, another inducer of apoptosis, unmasked a voltage-independent Ca2+ permeability as well. 3. A lower concentration of ionomycin (1 microM) did not induce apoptosis, and neither depolarized LNCaP cells nor produced the biphasic increase in [Ca2+]i. However, the first increment in [Ca2+]i due to release from internal Ca2+ stores was evident at this concentration of ionomycin. 4. Simultaneous recordings of [Ca2+]i and ion channel activity in the cell attached configuration of patch clamp revealed a Ca2+-permeable, Ca2+-independent, non-selective cation channel of 23 pS conductance. This channel was activated only during the second increment in [Ca2+]i induced by ionomycin. The absence of serum activated the 23 pS channel as well, albeit at a lower frequency than with ionomycin. 5. Thus, the 23 pS channel can be activated by two unrelated inducers of apoptosis and it could be another Ca2+ influx mechanism in programmed cell death of LNCaP cells.
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